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Physiologically relevant animal models of perinatal brain injury can advance our understanding of these influences and thereby provide opportunities to develop therapies and improve long-term outcomes.
A critical issue in animal models of perinatal brain injury is to adapt the pertinent pathophysiological scenarios to their corresponding developmental window in order to induce neuropathological and behavioral characteristics reminiscent to perinatal cerebral palsy (CP).
Melatonin has also some benefits in other "toxic models" of perinatal brain damage based on excitotoxic cascade [4].
Further preclinical studies are needed to confirm the ability of iNO to induce neuroprotection in other animal models of perinatal brain damage.
However, traditional epidemiologic and obstetric models of perinatal death do not support this iatrogenic increase in early delivery [ 11- 14].
A variety of drugs targeting cell death pathways have been tested in animal models of perinatal brain injury.
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We have designed a clinically relevant model of perinatal asphyxia providing intrapartum hypoxia in rats.
We hypothesized that docosahexaenoic acid pretreatment would improve function and reduce brain volume loss in this rat model of perinatal brain injury and inflammation.
We hypothesized that pretreatment with docosahexaenoic acid (DHA), a potentially neuroprotective polyunsaturated fatty acid, would improve function and reduce brain damage in a rat model of perinatal hypoxia-ischemia.
To test these hypotheses, we chose a well-known animal model of perinatal asphyxia.
We used an animal model of perinatal asphyxia, in which rat pups were exposed to 15 min of intrauterine anoxia during Cesarean section birth.
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